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• W2013033367 abstract "Purpose The transcription factor subunit hypoxia-inducible factor-1α (HIF-1α) is currently discussed as a potential endogenous marker of tumor hypoxia to select patients for modified treatment. Despite an association of immunohistochemical HIF-1α overexpression and poor prognosis after radiotherapy in many tumor entities, the reported pattern of HIF-1α staining was often not consistent with tumor hypoxia. To explain this discrepancy, we studied the in vitro conditions under which HIF-1α protein accumulates. Methods and materials FaDu human pharyngeal carcinoma and HT 1080 human fibrosarcoma cells were treated with different schedules of in vitro hypoxia at 5%, 1%, and 0.1% O2 and reoxygenation. HIF-1α protein levels were determined in nuclear extracts. Cellular radiation sensitivity was assessed by clonogenic survival assay after single-dose irradiation at the above oxygen concentrations. Results In both cell lines, weak HIF-1α expression was observed at 20% O2 and after 10 min of hypoxia. Increased HIF-1α protein levels were observed at 1 h of hypoxia, remained stable over 24 h, and decreased to baseline within 15 min of reoxygenation. HIF-1α protein at 5% O2 was half-maximal in FaDu but indistinguishable from 0.1% O2 in HT 1080. A good correlation of HIF-1α protein level and hypoxic radiation resistance, with equal ranking of data points by both assays, was observed in FaDu cells but not in HT 1080 cells. Conclusions The ability of HIF-1α to indicate radiobiologically relevant levels of tumor hypoxia seems to be cell type specific. This finding may explain the inconsistent results regarding the pattern of HIF-1α expression in tumor sections." @default.
• W2013033367 created "2016-06-24" @default.
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• W2013033367 date "2004-03-01" @default.
• W2013033367 modified "2023-10-11" @default.
• W2013033367 title "Cell type–specific association of hypoxia-inducible factor-1α (HIF-1α) protein accumulation and radiobiologic tumor hypoxia" @default.
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• W2013033367 doi "https://doi.org/10.1016/j.ijrobp.2003.11.030" @default.
• W2013033367 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15001269" @default.
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